DENis Titov

Denis Titov, PhD, Assistant Professor, Department of Metabolic Biology & Nutrition, Department of Molecular & Cell Biology, University of California, Berkeley

Research Description: Our lab develops experimental and computational approaches to achieve a predictive understanding of metabolism — how it is controlled, why it is organized the way it is, and how it breaks down in aging and disease. One current research effort in the lab combines modeling and experiments to uncover the function of allosteric feedback regulators of metabolic enzymes. Applied to glycolysis, this approach revealed the cellular function of classical allosteric regulators whose roles had remained unknown since their discovery in the 1950s. The lab is now building a model of hepatocyte glucose metabolism to determine which enzyme activities drive excessive hepatic glucose production in type 2 diabetes and to predict which enzymes a drug should target. In a complementary effort, the laboratory develops genetically encoded tools that directly manipulate the ATP/ADP, NAD+/NADH, and NADP+/NADPH ratios and mitochondrial membrane potential in living cells. These tools allow researchers to establish causal links between cellular energy state and physiology, and the lab is applying them to insulin secretion by beta cells.

Selected relevant publications (SDRC members in BOLD):

  1. Choe M, Einav T, Phillips R, Titov DV. Glycolysis model shows that allostery maintains high ATP and limits accumulation of intermediates. Biophysical Journal. 2025 May 20;124(10):1562-1586.

  2. Kober MM, Yang X, Webb BA, Titov DV. F26BP enables control of glycolysis rate independent of energy state. bioRxiv 2026.01.31.703051.

  3. Ekvik AE, Kober MM, Titov DV. Genetically encoded manipulation of ATP/ADP ratio in human cells uncovers proteomic and physiological signatures of energy stress. Cell Chemical Biology. 2026 May 21;33(5):683-698.

  4. Choe M, Ekvik AE, Stalnaker G, Shin HR, Titov DV. Genetically encoded tool for manipulation of ΔΨm identifies its role as the driver of ISR induced by ATP synthase dysfunction. Cell Chemical Biology. 2025 Apr 17;32(4):620-630